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目的为了探讨20-羟基蜕皮甾酮(20-hydroxyecdysone,20E)对Ⅰ型糖尿病小鼠降糖作用及相关机制。方法小鼠(体重20±2 g)随机分3组,用150 mg/kg腹腔注射链脲佐菌素造模,之后正常对照组和Ⅰ型糖尿病组小鼠灌服蒸馏水10 ml/kg;20E治疗组按5 mg/kg剂量灌服20E。药物干预3周后,观察肝脏形态学改变,测定血糖和肝脏糖原含量,分析糖酵解过程中的第一个限速酶—葡萄糖激酶和核心炎症因子—肿瘤坏死因子-α的表达。结果与Ⅰ型糖尿病组相比,20E处理后肝细胞损伤程度减轻;血糖浓度比Ⅰ型糖尿病组降低了92.7%(P<0.01),肝脏糖原含量增加了64.1%(P<0.05);Real-time PCR结果显示,20E处理后葡萄糖激酶m RNA水平增加了107.3%(P<0.01),肿瘤坏死因子-α表达水平降低了68.7%(P<0.05)。结论 20E具有降低Ⅰ型糖尿病小鼠血糖的作用,其机制可能与诱导肝脏葡萄糖激酶表达、增加肝脏糖原储备和增强肝脏保护作用有关。
Objective To investigate the hypoglycemic effect of 20-hydroxyecdysone (20E) on type 1 diabetic mice and its related mechanism. Methods Mice (weighing 20 ± 2 g) were randomly divided into three groups. The mice were injected with streptozotocin at a dose of 150 mg / kg. After that, the mice in the normal control group and type Ⅰ diabetic group were given distilled water (10 ml / kg) The treatment group was fed with 20E at a dose of 5 mg / kg. Three weeks after drug intervention, morphological changes of liver were observed. Blood glucose and liver glycogen contents were measured. The expression of the first rate-limiting enzyme, glucokinase and core inflammatory factor-tumor necrosis factor-α, was analyzed. Results Compared with type Ⅰ diabetes group, the degree of hepatocyte injury was relieved after 20E treatment. The blood glucose level decreased 92.7% (P <0.01) and the liver glycogen content increased 64.1% (P <0.05) compared with type Ⅰ diabetes mellitus group. The results of -time PCR showed that the level of glucokinase m RNA increased by 107.3% (P <0.01) and the expression of TNF-α decreased by 68.7% (P <0.05) after 20E treatment. Conclusion 20E can reduce the blood glucose in type 1 diabetic mice. The mechanism may be related to the induction of hepatic glucokinase expression, increase of liver glycogen reserves and enhancement of liver protection.